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Biomedical subjects

R F Garry

Publications and source records attributed to R F Garry.

89 records · Page 5Linked to original sources
PubMed1985

Inhibition of hepatic phosphoenolpyruvate carboxykinase by avian reticuloendotheliosis viruses.

Severe weight loss is associated with many malignant diseases of humans and animals. Avian reticuloendotheliosis viruses (RE viruses) induce runting in experimentally infected chickens. Chickens infected with a replication-competent RE virus, reticuloendotheliosis-associated virus, weighed 30-50% less than control birds at the time of death. Chickens infected with reticuloendotheliosis virus, a replication-defective acute leukemia virus, weighed 30% less than the controls. The runting induced by RE viruses does not occur because of reduced food intake. Activities of phosphoenolpyruvate carboxykinase, a key gluconeogenic enzyme in the liver, were reduced approximately 40 and 50%, respectively, by infection with reticuloendotheliosis-associated virus and reticuloendotheliosis virus. RE virus infection, however, did not affect the hepatic pyruvate carboxylase activity, indicating that inhibition of phosphoenolpyruvate carboxykinase is not due to a general inhibition of all liver enzymes. Birds given injections of UV-inactivated RE viruses or reticuloendotheliosis virus-transformed, non-virus-producing tumor cells also exhibited a reduction in phosphoenolpyruvate carboxykinase activity.

Animals↗
PubMed1984

Alterations in monovalent cation transport in Sindbis virus-infected chick cells.

Influx experiments using the potassium tracer 86Rb+ indicated that the activity of the Na+K+ ATPase, or sodium pump, was reduced 40-50% as a consequence of Sindbis virus infection of avian fibroblasts. The inhibition of this ouabain-sensitive, active transport system temporally correlated with a decrease in the intracellular K+ concentration and the termination of cellular protein synthesis. By contrast, the rate of influx facilitated by the furosemide-sensitive (Na+K+Cl-) cotransport system was only slightly depressed. Efflux experiments indicated that no alterations in the relative rate of nonspecific permeability or "leakage" of K+ could be detected in chick cells infected by Sindbis virus. The amount of [3H]ouabain bound to Sindbis virus-infected cells paralleled the reduction in Na+K+ ATPase activity. These binding studies revealed no difference in the number of Na+ pump sites. The Km of ouabain binding, however, increased approximately 3.5-fold in the virus-infected cells. No change in the apparent affinity of the Na+ pump for K+ could be detected, yet the Vmax for ouabain-sensitive K+ transport was decreased. These experiments suggest that a reduction in Na+K+ ATPase turnover results in the altered intracellular monovalent cation levels found in Sindbis virus-infected chick cells.

Animals↗
PubMed1983

Induction of stress proteins in Sindbis virus- and vesicular stomatitis virus-infected cells.

Two proteins which are related to certain proteins induced by hyperthermia (heat shock proteins; hsp) are synthesized during lytic infection of chick embryo (CE) cells by Sindbis virus or vesicular stomatitis virus (VSV). Incubation of the infected cells at elevated temperature further increased the rate of synthesis of these proteins. The stress proteins induced by Sindbis virus had different mobilities on SDS-polyacrylamide gels compared to related stress proteins induced in mock-infected CE cells. Induction of the stress proteins in Sindbis virus- and VSV-infected CE cells was actinomycin D sensitive. Kinetic studies indicated that induction of the stress proteins is an early event during infection. The lytic virus-induced selective termination of host protein synthesis did not affect the synthesis of these proteins. Furthermore, the synthesis of these virus-induced stress proteins was resistant, relative to the synthesis of most host proteins, to alterations in the intracellular concentrations of Na+ and K+. The synthesis of a protein related to a major low-molecular-weight hsp of CE cells was not induced after Sindbis virus or VSV infection. Immunoprecipitation experiments and sedimentation analyses demonstrated that significant levels of the capsid protein (C) of Sindbis virus and nucleocapsid protein (N) of VSV are physically associated with a hsp in lysates of infected CE cells.

Amino Acids↗
PubMed1982

Membrane-mediated alterations of intracellular Na+ and K+ in lytic-virus-infected and retrovirus-transformed cells.

Infection of chick-embryo fibroblasts and other cells by certain animal viruses results in alterations in the intracellular concentrations of Na+ and K+. Dramatic alterations in monovalent-cation concentrations of lytic-virus-infected cells may favor the synthesis of viral proteins over cellular proteins. More subtle alterations in retrovirus-transformed cells may result in the expression of many morphological and biochemical changes associated with the transformed phenotype.

Animals↗
PubMed1981

Avian reticuloendotheliosis virus: identification of the hematopoietic target cell for transformation.

Non-virus-producing hematopoietic cells transformed in vitro by reticuloendotheliosis virus (REV-T) induce lethal "reticuloendotheliosis" when inoculated into histocompatible chickens. This is the first direct demonstration that an in vivo target cell of an avian acute leukemia virus can be transformed in vitro. The tumorigenic, REV-T-transformed non-virus-producing cells fail to express helper-virus-coded proteins. REV-T transformed tumorigenic cells therefore do not require helper-virus functions. Cells transformed in vivo or in vitro by REV-T have lymphoblastoid morphology and express low levels of terminal-deoxynucleotidyl-transferase activity and bursal-cell determinants. One clone synthesized Ig mu. The preferred target cells for REV-T transformation are therefore immature lymphoid cells that express B-cell determinants. We propose that the unique transforming sequence of REV-T be designated rel (lymphoid).

Animals↗
PubMed1979

Effect of Sindbis birus infection on survival of mice in the cold.

Mice infected with 10(9) plaque-forming units (PFU) of Sindbis virus 9 h prior to exposure to cold (5 degrees C) died more rapidly after entering the new environment than saline-injected control mice. The early deaths occurred in animals singly housed without bedding and only when food was withheld. Because deaths could be prevented by providing the infected animals with food, it was concluded that metabolic alteractions resulting from the virus infection were responsible for the deaths. As evidence, corticosteroid-inducible hepatic enzymes did not respond to hydrocortisone administration in virus-infected mice housed at 5 degrees C. Phosphoenolpyruvate carboxykinase (PEPCK) (EC 4.1.1.32) was induced significantly in control mice held at 5 degrees C for 5 h, but failed to induce in infected mice in the cold. Tryptophan oxygenase (TO) (EC 1.13.11.11) activity was also induced in control mice at 5 degrees C, but was too low to be measured in livers of all infected mice including those exposed to cold. The conclusion that Sindbis virus-infected mice were unable to make the metabolic adjustments required for survival at 5 degrees C was further indicated by severe hypoglycemia and rapid drop in rectal temperature that occurred in infected mice after 5 h in the cold.

Animals↗
PubMed1978

Effect of low-NaCl medium on the envelope glycoproteins of Sindbis virus.

Lowering the NaCl concentration of the medium inhibits the release of Sindbis virus from infected chicks cells at a stage after the nucleocapsids have bound to the membranes of the infected cells. The failure of trypsin treatment to release the inhibited virus and the ratio of the proteins in the inhibited cells make it seem likely that the inhibited virus is all intracellular. Experiments using antisera specific for E1 and E2, the envelope glycoproteins of Sindbis, suggest that the inhibitory effect of low-salt medium is mediated through an effect on E2. Lactoperoxidase radioiodination experiments indicate that, even when cleaved from PE2, E2 is not exposed on the surface of low-NaCl-treated chick cells.

Cell Line↗
PubMed1976

Effect of medium of lowered NaCl concentration on virus release and protein synthesis in cells infected with reticuloendotheliosis virus.

When cultures producing reticuloendotheliosis virus were incubated for 24 h in medium of lowered NaCl concentration, virus production was inhibited. The extent of inhibition increased as the salt concentration of the medium was decreased. The inhibition was rapidly reversed by replacement of low-salt medium with normal medium. During the first hour after the inhibited cultures were returned to normal medium, virus was released at an accelerated rate, making the total amount of virus released by inhibited and control cultures the same. After 1 h in normal medium, the rate of virus production in the previously inhibited cultures was the same as in the control cultures. Incubation of infected cells in low-salt medium resulted in a 60% decrease in the overall rate of protein synthesis. Although returning the cells to normal medium rapidly reversed the inhibition of virus production, it did not rapidly increase the rate of protein synthesis. These results suggest that host cell-directed protein synthesis is preferentially inhibited by the low-ionic-strength medium, whereas that required for virus production continues.

Animals↗
PubMed1974

Interferon induction by poly (I): poly (C) enclosed in phospholipid particles.

Liposomes were prepared with phospholipids (sphingomyelin, lecithin, and phosphatidylethanolamine) in combination with cholesterol and charged lipids (dicetyl phosphate and stearylamine) and contained either poly(I):poly(C) or poly(I). Neutral and positively charged liposomes attached much better to L-929 cells in tissue culture than did negatively charged particles. Liposomes were toxic to L cells at relatively low concentrations, making the determination of antiviral activity induced by particles containing poly(I):poly(C) difficult to measure by the plaque reduction assay. When injected into mice, all of the liposomes containing poly(I):poly(C), except phosphatidylethanolamine liposomes, greatly potentiated and extended the serum interferon response of poly(I):poly(C). Lecithin and sphingomyelin liposomes given intravenously were ten times more effective than free poly(I):poly(C) in stimulating production of serum interferon. Sphingomyelin liposomes containing [(14)C]poly(I):poly(C) were 88% cleared from the bloodstream of mice by 3 min after intravenous injection. Most of the radioactivity (70%) was captured by the liver and remained there for at least 4 h. By 2 h, 7% of the radioactivity could be found in the spleen. Five percent of the radioactivity was found in the lungs at 30 min, with decreasing amounts thereafter. Small amounts of radioactivity were found in the muscle and kidneys. The spleen was shown to contain appreciable levels of interferon at 4 h, and low levels were found in the liver. Radioactivity accumulated slowly in the liver following an intraperitoneal injection of sphingomyelin liposomes containing [(14)C]poly(I):poly(C). By 4 h, 26% of the dose was recovered from the liver and 4.9% from the spleen, with small amounts in the lung, kidney, and omentum.

Animals↗